Ezetimibe Completely Replaced LDL-Apheresis for the Treatment of Familial Hypercholesterolemia and Coronary Artery Disease after CABG—A Case Report

Ikuo Yokoyama

Department of Cardiovascular Medicine, Clinical Research Center, Sanno Medical Center Hospital, International University of Health and Welfare, Tokyo, Japan.

DOI: 10.4236/jbise.2013.62A028                

Abstract

Intensive treatment of hyperlipidemia is an important factor in the prevention of cardiovascular disease. Among several therapies, statins are well recognized as playing a central role, although low density lipoprotein bound cholesterol-apheresis can be used to treat very severe cases of familial hypercholesterolemia. However, statins are not always effective on their own and, recently, ezetimibe has emerged as a unique anti- hypercholesterolemic drug that acts as a cholesterol transporter inhibitor; its role is only partially understood. I experienced rare case that appeared to benefit from ezetimibe therapy, and report them as they help increase our knowledge of this novel drug.

Keywords

Ezetimibe; Familial Hypercholesterolemia; Statins; LDL-Apheresis; Coronary Artery Disease

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1]	De Lorgeril, M., Renaud, S., Mamelle, N., et al. (1994) Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet, 343, 1454 1459. doi:10.1016/S0140-6736(94)92580-1
[2]	Scandinavian Survival Study Group (1994) Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease. Lancet, 344, 1383-1389.
[3]	Shepherd, J., Cobbe, S.M., Ford, I., et al. (1995) Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. New England Journal of Medicine, 333, 1301-1307. doi:10.1056/NEJM199511163332001
[4]	The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group (1998) Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. New England Journal of Medicine, 339, 1349-1357. doi:10.1056/NEJM199811053391902
[5]	Lewis, S.J., Sacks, F.M., Mitchell, J.S., et al. (1998) Effect of pravastatin on cardiovascular events in women after myocardial infarction: the cholesterol and recurrent events (CARE) trial. Journal of the American College of Cardiology, 32, 140-146. doi:10.1016/S0735-1097(98)00202-2
[6]	Gould, K.L., Ornish, D., Kirkeeide, R., et al. (1992) Improved stenosis geometry by quantitative coronary arte riography after vigorous risk factor modification. American Journal of Cardiology, 69, 845-853. doi:10.1016/0002-9149(92)90781-S
[7]	Pitt, B., Waters, D., Brown, W.V., et al. (1999) Aggressive lipid-lowering therapy compared with angioplasty in stable coronary artery disease. Atorvastatin versus revas cularization treatment investigators. New England Journal of Medicine, 341, 70-76. doi:10.1056/NEJM199907083410202
[8]	Ge, L., Wang, J., Qi, W., et al. (2008) The cholesterol absorption inhibitor ezetimibe acts by blocking the sterol induced internalization of NPC1L1. Cell Metabolism, 7, 508-519. doi:10.1016/j.cmet.2008.04.001
[9]	Stein, E., Stender, S., Mata, P., et al. (2004) Achieving lipoprotein goals in patients at high risk with severe hypercholesterolemia: Efficacy and safety of ezetimibe co administered with atorvastatin. American Heart Journal, 148, 447-455. doi:10.1016/j.ahj.2004.03.052
[10]	Gordon, B.R., Kelsey, S.F., Dau, P.C., et al. (1998) Long-term effects of low-density lipoprotein apheresis using an automated dextran sulfate cellulose adsorption system. Liposorber Study Group. American Journal of Cardiology, 81, 407-411. doi:10.1016/S0002-9149(97)00947-8
[11]	Thompson, G.R., Barbir, M., Davies, D., et al. (2010) Efficacy criteria and cholesterol targets for LDL apheresis. Atherosclerosis, 208, 317-321. doi:10.1016/j.atherosclerosis.2009.06.010
[12]	Lally, S., Tan, C.Y., Owens, D. and Tomkin, G.H. (2006) Messenger RNA levels of genes involved in dysregulation of postprandial lipoproteins in type 2 diabetes: The role of Niemann-Pick C1-like 1, ATP-binding cassette, transporters G5 and G8, and of microsomal triglyceride transfer protein. Diabetologia, 49, 1008-1016. doi:10.1007/s00125-006-0177-8